We have so far established that lipoprotein lipase (LPL) is present in the lung in significant concentrations and that it hydrolyzes lipoprotein-triglyceride. Lung LPL shows preference for certain fatty acids. Its secretion might be hormonally regulated. Recently we have shown that LPL appears in the lung at a certain point in gestation and that Intralipid clearance is impaired in the premature infant. Present work is focused on the role of LPL in remodeling of lipoprotein remnants. In addition to continuing the research along these lines, we propose to study: 1) The origin of LPL in the lung (identification of the source in the tissue); 2) Species differences in LPL; 3) The effect of hyperoxia on LPL function. We also want to elucidate further the relative contribution and interaction of free fatty acids and triglycerides to lung energy and surfactant metabolism. Most of these studies will continue to utilize the isolated ventilated-perfused lung as the model to obtain the answers. The major significance of this work is: 1) LPL is emerging as an important enzyme in lung lipid metabolism; 2) LPL might be an important marker of endothelial damage; 3) LPL might play an important role in remodeling circulating lipoproteins. This research might, therefore, lead to important insight into the mechanims involved in pulmonary vascular disorders, atherosclerosis and nutritional disorders.